These inflammatory mediators cause vasodilation and increase vascular permeability, resulting in plasma extravasation into the skin, subcutaneous tissues, and submucosa . by the contact activation pathway. These inflammatory mediators cause vasodilation and increase vascular permeability, resulting in plasma extravasation into the skin, subcutaneous tissues, and submucosa . Normally, ACE will degrade bradykinin and substance P prior to the development of life-threatening angioedema; however, this protective mechanism is inhibited by ACE-i therapy (Figure ?(Figure66). ACE-i angioedema accounts for one-third of all angioedema-related visits Acta2 to the emergency department (ED)  and is associated with a 0.7% incidence rate within the first month of prescription and 0.23% within one year . Incidence Briciclib peaks within the first month of treatment, with the risk of angioedema decreasing significantly after 9-12 weeks . However, it is important to note that the risk of ACE-i angioedema persists even after many years of use [2,3]. We present a case series to illustrate the imaging manifestations specific to ACE-i angioedema of the head and neck.? This article was previously presented as a meeting abstract at the 2020 European Congress of Radiology Summit in July 2020 (DOI: 10.26044/ecr2020/C-15054). Case presentation Institutional Review Board (IRB) approval for the study was obtained from the University of Florida Health IRB committee prior to conducting retrospective chart reviews (IRB202100494). Informed consent requirements were waived. We used the mPower search engine to look for ACE-i angioedema and identified 30 patients with the descriptive characteristics of the condition in their imaging reports. Based on the chart review, five patients were deemed to be clinically diagnosed with ACE-i angioedema. No identifying information is included in the following case descriptions or figures. Case 1 A 62-year-old African American Briciclib male with a history of hypertension on ramipril, initiated six weeks prior, presented with physical findings of swelling of the face, lips, and tongue. The patient had previously taken a medication, which had made him swell all over his body, and had been subsequently advised to avoid taking that medication. He could not remember the name of the medication that had caused these symptoms previously. At that time, he had been treated with antihistamines, steroids, and a proton pump inhibitor. On this presentation, his blood pressure was noted to be 187/90 mmHg, and WBC was elevated at 12.7. The remainder of the vital signs and lab values were normal. Over the course of two hours in the ED, the patient was noted to have a progression of the lip and oral cavity mucosal swelling and underwent oral rapid sequence intubation (RSI) with a video laryngoscope. He was found to have vocal cord edema. A CT of the neck was ordered to evaluate for structural lesions (Figure ?(Figure1).1). The patient was treated with intravenous (IV) methylprednisolone Briciclib and diphenhydramine and extubated one day later with complete resolution of symptoms. Figure 1 Open in a separate window Coronal and axial enhanced CTA: Coronal enhanced CT demonstrating buccal mucosal swelling bilaterally representing angioedema (orange outline). B: Axial enhanced CT demonstrating findings of superficial and deep subcutaneous fat stranding representing subcutaneous angioedema (orange arrows). Evaluation of the tongue was limited due to beam hardening from dental amalgam and distortion from the endotracheal tube CT:?computed tomography Case 2 A 59-year-old African American male with a history of hypertension on lisinopril, initiated three days prior, presented with worsening dysphagia, sore throat, and shortness of breath for 24 hours. He also complained of a muffled voice and was noted to have tachypnea and tachycardia. He was normotensive at presentation. The patient received epinephrine upon presentation. He demonstrated a prominent uvula and underwent emergent nasal intubation for respiratory distress with a video laryngoscope, at which time his true vocal cords were noted as swollen. The epiglottis was also noted.